A patent upper airway is a basic requirement for breathing. This, of course, also holds true for breathing during sleep. It has recently been described that such patency—and thus breathing—may be partially or totally interrupted during sleep due to a collapse or obstruction of the upper airway; it should be observed that obstruction, in the context of the present invention, excludes obstruction by foreign objects or by material excreted by the body, such as mucus. In its simplest form partial airway collapse or obstruction is indicated by profound and vigorous snoring. More pronounced collapse or obstruction results in hypopnea, a condition in which airflow is reduced during inspiration with or without concomitant signs of hypoxemia. The condition of total collapse of the upper airway is referred to as obstructive sleep apnoea (OSA). This condition is associated with repeated episodes of interrupted airflow in spite of inspiratory attempts, resulting in hypoxemia, hemodynamic changes and arousal from sleep. Sleep fragmentation, hypoxia and/or other OSA phenomena yet unidentified are likely to lead to typical daytime symptoms such including hypersomnolence, cognitive disturbance, reduced working and driving performance, depression and loss of memory. Moreover, cardiovascular complications, in particular hypertension, cardiac failure, myocardial infarction and stroke are common in OSA and OSA has been associated with increased insulin resistance, diabetes, obesity, changes in lipid metabolism and increased platelet aggregability. Such symptoms and complications are not confined to severe cases but also observed in cases of partial OSA.
The prevalence of OSA in the adult population is in the order of 10-12%. The prevalence of OSA in combination with pronounced daytime symptoms in the order of 1-3%. The prevalence of minor daytime symptoms induced by discrete sleep-related breathing disturbances is unknown. However, habitual snoring is a common phenomenon reported by 15-25% of the adult population.
The patophysiology of OSA is virtually unknown. Though a number of predisposing factors have been identified, e.g. obesity, hypertrophied tissue in the upper airway (particularly in children), and short jaw, there is a large number of OSA prone individuals lacking these factors.
The absence of observable aberrant anatomic factors, however, does not exclude a dynamic malfunction of the tongue and the upper airway dilating musculature. Such defect function may originate in the central nervous system, at the level of signal transmission to peripheral muscles or at the neuromuscular junction. It is well known and has been reported in the literature that electromyographically recorded signal from the lingual muscles (submental EMG) may be attenuated or even disappear in association with obstructive apnoeas. This defective control seems to be particularly pronounced during sleep only, suggesting the central nervous, peripheral neural and/or neuromuscular control of the upper airway is particularly prone to be affected in this state.
The principal forms of treatment in OSA are surgery of the upper airway, intraoral mandibular advancement devices and long-term treatment with nasal continuous positive airway pressure (nCPAP). These methods of treatment are cumbersome and expensive. Various forms of pharmacological treatment, e.g. by administration of tricyclic anti-depressants, theophylline, progesterone, have been employed but have not gained wide clinical use.